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e-mail- dgoebel@med.wayne.edu
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Education:
Central Michigan University, B.S. 1978, Biology
Wayne State University, equiv. B.S., 1984, Chemistry
Wayne State University, M.S., 1988, Chemistry
Wayne State University, Ph.D., 1991, Anatomy & Cell Biology
Training:
| 1991-92 | Research Associate,
Center for Cell Biology, Laboratory of Neuro-molecular Biology, Sinai Hospital, and Dept. of Psychiatry, Wayne State University, School of Medicine, Detroit, MI. |
| 1992-93 | Research Associate,
Dept. of Anatomy/Cell Biology, Wayne State University, School of Medicine, Detroit, MI. |
Faculty Appointments:
| 1993-96 | Assistant Professor
(Research), Dept. Anatomy/Cell Biology, Wayne State University School of Medicine, Detroit, Michigan. |
| 1996-2003 | Assistant Professor
(Tenure trac), Dept. Anatomy/Cell Biology, Wayne State University School of Medicine, Detroit, Michigan. |
| 2003- | Associate Professor
(Tenured), Dept. Anatomy/Cell Biology, Wayne State University School of Medicine, Detroit, Michigan. |
| 1989-90 | Visual Science Training
Fellowship (National research service award for the NIH), Wayne State University. |
Major Research Interests:
Neuroscience, molecular neurobiology focusing on neurotoxicity/neuroprotection
mechanisms and neurochemical and receptor interactions in the mammalian retina.
Current Research:
 NMDA receptors have been widely implicated as mediators of necrosis and apoptosis following excitotoxic insult. Both processes have been described in the retina where they are linked to the clinical disorders of ischemia and glaucoma, respectively. Although necrosis and apoptosis can be effectively blocked by a variety of NMDA-receptor antagonists, the underlying mechanisms involved in the initiation and propagation of these events is not fully resolved. Using rat retinal models, we are investigating the mechanisms through which NMDA-induced toxicity leads to necrotic and apoptotic cell death. We hypothesize that initiation of both necrosis and apoptosis is linked to activation of specific subunits of the NMDA receptor, but that beyond this point, the two processes diverge. To test this hypothesis we have directed our studies to: 1) compare necrotic and apoptotic models of retinal cell death with regard to their correlation with subunits of the NMDA receptor; 2) determine the effect of NMDA antagonists on the expression of NMDA-induced excitotoxicity in necrotic and apoptotic models; 3) determine the role of GABA in mediating NMDA-induced necrosis and apoptosis in the retina. These studies utilize molecular and biochemical methods to determine levels of NMDA receptor subunit gene and protein expression. Immunocytochemical and morphological techniques are being used to examine the effects of agonist or antagonist application on cell number. Elucidation of the mechanisms of NMDA-mediated toxicity may provide new insight regarding the applicability of specific drugs for treating necrotic and apoptotic visual disorders. Click here to view the larger image. |
References
| 1. | Goebel, D.J., and Winkler, B.S. (2006). Blockade of PARP activity attenuates poly(ADP-ribosyl)ation but offers only partial neuroprotection against NMDA-induced cell death in the rat retina. J. Neurochem. 98:1732-1745. Medline |
| 2. | Goebel, D.J. and Poosch, M.S., (2001). Transient down-regulation of NMDA receptor subunit gene expression in the rat retina following NMDA-induced neurotoxicity is attenuated in the presence of the non-competitive NMDA receptor antagonist MK-801. Exp.Eye Res., 72:547-558. Medline |
| 3. | Pourcho, R.G., Pu. Q. and Goebel, D.J., (2001). Cellular and subcellular distribution of NMDA receptor subunit NR2B in the retina. J. Comp. Neurol., 433: 75-85. Medline |
| 4. | Goebel, D.J. and Poosch, (1999) M.S. NMDA receptor subunit gene expression in the rat brain: A quantitative analysis of endogenous mRNA levels of NR1Com, NR2A, NR2B, NR2C, NR2D and NR3A. Mol. Brain Res. 69:164-170. Medline |
| 5. | Goebel, D.J., Aurelia, J.L., Jojich, L. Tia, Q., and Poosch, M.S. (1998). Immunocytochemical localization of the NMDA-R2A receptor subunit in the cat retina. Brain Res. 808:141-154. Medline |
| 6. | Goebel, D.J. and Pourcho, R.G. (1997) Calretinin in the cat retina: Colocalizations with other calcium-binding proteins, GABA and glycine. Vis. Neurosci. 14:311-322. Medline |
| 7. | Goebel, D.J. (1996). Quantitative gene expression of two types of glycine transporter in the rat CNS. Mol. Brain Res. 40:139-142. Medline |
| 8. | Bannon, M.J., Poosch, M.S., Xia, Y. Goebel, D., Cassin, B. and Kapatos, G. (1992). Dopamine transporter mRNA content in human substantia nigra decreases precipitously with age. Proc. Natl. Acad. Sci. 89:7095-7099 Medline |
| 9. | Goebel, D.J. and Pourcho, R.G. (1992). Hydrolysis of substance P in the rabbit retina: II. The role of a membrane-associated acetylcholine-sensitive metalloendopeptidase. An in vitro study. Neuropeptides 21:35-48. Medline |
| Pourcho, R.G. and Goebel, D.J. (1990).
Autoradiography and immunocytochemical studies of glycine containing neurons
in the retina. In: Glycine Neurotransmission. Eds., Ole
P. Otterson and Jon Storm-Mathisen, John Wiley & Sons Limited,
p. 355-389.
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